Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.
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Summary
RANKL selectively induces NFATc1 expression via TRAF6 and c-Fos signaling pathways, and may represent a master switch for regulating terminal differentiation of osteoclasts, functioning downstream of RANKL.
- Type
- article
- Published
- 2002-12-01
- Cited by
- 2,500
- References
- 61
- Access
- Open access
- OpenAlex
- https://openalex.org/W2017372504
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:39768760
Keywords
RANKL, Cell biology, NFAT, Biology, Transcription factor
References
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- Genetic control of skeletal development.
- Role of the NF-ATc transcription factor in morphogenesis of cardiac valves and septum
- T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-γ
- Calcium oscillations increase the efficiency and specificity of gene expression
- Structure of the DNA-binding domains from NFAT, Fos and Jun bound specifically to DNA
- Bone resorption by osteoclasts.
- Conditional requirement for the Flk-1 receptor in the in vitro generation of early hematopoietic cells.
- Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes.
- Gene expression elicited by NFAT in the presence or absence of cooperative recruitment of Fos and Jun
- c-Fos: a key regulator of osteoclast-macrophage lineage determination and bone remodeling.
- Medicine: Interfering with bone remodelling
- Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.
- Early Events in M-CSF Receptor Signaling
- Segregation of TRAF6‐mediated signaling pathways clarifies its role in osteoclastogenesis
Cited by
- Molecular and cellular basis of bone resorption
- Signal transduction by receptor activator of nuclear factor kappa B in osteoclasts.
- Transcriptional control of receptor activator of nuclear factor-kappaB ligand by the protein kinase A activator forskolin and the transmembrane glycoprotein 130-activating cytokine, oncostatin M, is exerted through multiple distal enhancers.
- Osteoclast differentiation and gene regulation.
- Deubiquitinating enzyme CYLD negatively regulates RANK signaling and osteoclastogenesis in mice.
- RANKL-induced schlafen2 is a positive regulator of osteoclastogenesis.
- Inhibition of the classical NF-κB pathway prevents osteoclast bone-resorbing activity
- Signal adaptor DAP10 associates with MDL-1 and triggers osteoclastogenesis in cooperation with DAP12
- Saurolactam inhibits osteoclast differentiation and stimulates apoptosis of mature osteoclasts
- Innate Immune-Like Function of Osteogenic Cells and Their Effects on Inflammatory Osteolysis
- Regulatory mechanism of osteoclastogenesis by RANKL and Wnt signals.
- Osteocyte Control of Osteoclastogenesis
- Osteoclast migration, differentiation and function: novel therapeutic targets for rheumatic diseases.
- Inhibitory effects of obovatol on osteoclast differentiation and bone resorption.
- Anti-Osteoclastogenic Activity of Praeruptorin A via Inhibition of p38/Akt-c-Fos-NFATc1 Signaling and PLCγ-Independent Ca2+ Oscillation
- Notch pathway inhibition controls myeloma bone disease in the murine MOPC315.BM model
- Acceleration of bone regeneration by local application of lithium: Wnt signal-mediated osteoblastogenesis and Wnt signal-independent suppression of osteoclastogenesis.
- [Osteoclast biology and osteoimmunology].
- Attenuated RANKL-induced cytotoxicity by Portulaca oleracea ethanol extract enhances RANKL-mediated osteoclastogenesis
- Epigenetic Regulation of Bone cells
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